C albicanshost Interaction from the Fungal Point of View

Transcript profiling experiments have been carried out to investigate gene expression changes occurring when C. albicans interacts with macrophages (Lorenz et al., 2004), neutrophils (Rubin-Bejerano et al., 2003; Fradin et al., 2005), or whole blood (Fradin et al., 2005). Lorenz et al. (2004) demonstrated changes in transcription occurring when C. albicans is phagocytosed by macrophages (Lorenz et al., 2004). In the early phase, the cells demonstrated starvation responses, but in later stages switched to hyphal growth and switched to glycolytic growth. C. albicans cells also demonstrated induction of oxidative stress responses (Lorenz et al., 2004). In a murine model of systemic candidiasis, GFP-promoter fusions confirmed that the glyoxylate cycle and gluconeogenic genes were induced following phagocytosis by macrophages and neutrophils (Barelle et al., 2006). However, the majority of cells in an infected kidney were of hyphal morphology and expressed glycolytic genes, not glyoxylate and gluconeogenic genes (Barelle et al., 2006).

C. albicans incubated with different blood fractions showed differing behaviours (Fradin et al., 2005). Transcript profiling showed that the profile obtained for C. albicans exposed to whole blood that was not reflective of all of the other different blood fractions. C. albicans exposed to red blood cells, mononuclear cells, plasma, or blood lacking neutrophils were active and rapidly switched to filamentous growth. In mononuclear cells C. albicans again showed induction of genes associated with hyphal growth. However, when incubated with neutrophils, C. albicans showed growth arrest and changes in gene expression to overcome nitrogen and carbon starvation (Rubin-Bejerano et al., 2003; Fradin et al., 2005). Genes involved in overcoming oxidative stress were also induced. C. albicans incubated in whole blood showed similar transcript profiles to those incubated with neutrophils, suggesting that neutrophils play a key role in systemic candidiasis (Fradin et al., 2005).

Expression profiling has also been carried out during infection of Hep2 epithelial cells, which resulted in upregulation of ALS2 & 5, among others (Sandovsky-Losica et al., 2006). The expression profile during adherence to human epithelia has also been determined, with profiles obtained during adherence to epithelium being very different to that obtained for plastics (Sohn et al., 2006b). Genes showing adhesion-dependent induction of expression included the cell surface genes PRA1, PGA23, PGA7, and HWP1 (Sohn et al., 2006b).

Methodology for the removal of contaminating host material has recently been published, allowing transcript profiling of C. albicans cells from infected tissue to be carried out (Andes et al., 2005). Induced genes in vivo in the kidney of infected mice included several previously shown to be important for pathogenesis; secreted enzymes and morphology-associated genes (Andes et al., 2005).

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